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Hengyang, China

Changsha Medical University/College is located in Changsha, Hunan Province, China.Changsha Medical University/College , China's governmental medical university for undergraduates,was founded by the famous educator Binsheng He in 1989. It is situated in Changsha, capital of Hunan Province and was upgraded to a medical university for undergraduates in 2005 by Ministry of Education. CSMU is under the jurisdiction of Hunan People's Government and the professional guidance of the Department of Public Health of the government. CSMU is listed in WHO's World Directory of Medical Schools and is welcoming students from all over the world. Wikipedia.


Yang J.,Hunan City University | Li D.,Hainan Normal University | Peng L.,Changsha Medical University | Long K.,Hunan City University
Journal of Computational and Theoretical Nanoscience | Year: 2013

Based on the classification of the amino acid, the paper presents a mathematic representation of protein sequences, and then obtains a M matrix on the basis of mathematic expression. Then we computed the mathematic invariable according to the M matrix, namely five-dimensional feature vector. According to the angle between two vectors, we analyzed the similarity of 13 kinds of the original sequence of coronavirus N protein. With the software PHYLIP, we create a phylogenetic tree structure and compare the experimental results with the traditional one. The experimental results show that the mathematical model of this method is simple and have low computational complexity and better results. Such method of mathematic representation and similarity analysis of protein sequences is a new impetus for the comparison of protein sequences. Copyright © 2013 American Scientific Publishers. Source


Bao M.-H.,Changsha Medical University | Dai W.,Central South University | Li Y.-J.,Central South University | Hu C.-P.,Central South University
Canadian Journal of Physiology and Pharmacology | Year: 2011

It is proposed that myocardial cell apoptosis causes ventricular remodeling and heart failure. The aim of the present study was to determine the effects of rutaecarpine (Rut) on hypoxia-reoxygenation (H-R)-induced apoptosis in myocardial cell line H9c2, as well as the underlying mechanisms. Cultured H9c2 cells were exposed to hypoxia for 24 h, followed by 12 h reoxygenation. Rut (in concentrations of 0.1, 1, and 10 μmol/L) was added 1 h prior to H-R. Cell viability and lactate dehydrogenase were measured to evaluate the cell injuries. Apoptosis was evaluated by Hoechst 33258 staining and flow cytometry. NADPH oxidase activity was measured by assay kit; intracellular reactive oxygen species (ROS) generation was detected by 2′,7′-dichlorofluorescein diacetate; and Nox2, Nox4, and p47 phox mRNA and protein expression were analyzed by real-time PCR and Western blotting, respectively. The results showed that H-R significantly decreased cell viability and increased the lactate dehydrogenase release, as well as the apoptotic rate, concomitantly with enhanced NADPH oxidase activity. H-R also upregulated mRNA and protein expressions of Nox2, Nox4, and p47 phox and increased ROS production. Treatment with Rut markedly reversed these effects introduced by H-R. These results suggest that the protective effects of Rut against H-R-induced myocardial cell injury and apoptosis might, at least partly, be due to the inhibition of the NADPH oxidase - ROS pathway. Source


Bao M.-H.,Changsha Medical University | Zhang Y.-W.,Central South University | Lou X.-Y.,Central South University | Cheng Y.,Central South University | Zhou H.-H.,Central South University
PLoS ONE | Year: 2014

Lectin-like low-density lipoprotein receptor 1 (LOX-1) is a receptor for oxidized low density lipoprotein (oxLDL) in endothelial cells. The activation of LOX-1 by oxLDL stimulates the apoptosis and dysfunction of endothelial cells, and contributes to atherogenesis. However, the regulatory factors for LOX-1 are still unclear. MicroRNAs are small, endogenous, non-coding RNAs that regulate gene expressions at a post-transcriptional level. The let-7 family is the second microRNA been discovered, which plays important roles in cardiovascular diseases. Let-7a and let-7b were predicted to target LOX-1 39-UTR and be highly expressed in endothelial cells. The present study demonstrated that LOX-1 was a target of let-7a and let-7b. They inhibited the expression of LOX-1 by targeting the positions of 310-316 in LOX-1 39-UTR. Over-expression of let- 7a and let-7b inhibited the oxLDL-induced endothelial cell apoptosis, NO deficiency, ROS over-production, LOX-1 upregulation and endothelial nitric oxide synthase (eNOS) downregulation. Moreover, we found that oxLDL treatment induced p38MAPK phosphorylation, NF-kB nuclear translocation, IkB degradation and PKB dephosphorylation. Let-7a or let- 7b over-expression attenuated these alterations significantly. The present study may provide a new insight into the protective properties of let-7a and let-7b in preventing the endothelial dysfunction associated with cardiovascular disease, such as atherosclerosis. © 2014 Bao et al. Source


Chen L.-H.,Peking University | Chen L.-H.,Changsha Medical University | Lin Z.-B.,Peking University | Li W.-D.,Peking University
Acta Pharmacologica Sinica | Year: 2011

Aim: To study the effects of Ganoderma lucidum polysaccharides (Gl-PS) on methotrexate (MTX)-induced small intestinal damage in mice and the underlying mechanisms. Methods: BALB/c mice were used for in vivo study. The mice were administered with Gl-PS (50, 100, or 200 mg/kg, ig) for 10 d, and injected with MTX (50 mg/kg, ip) on d 7 and 8 to induce intestinal damage, and then sacrificed on d 11 for morphological study and tissue malondialdehyde (MDA) and superoxide dismutase (SOD) measurements. Before sacrificing, blood samples were collected to analyze immunoglobulin A (IgA). Rat intestinal IEC-6 cells were used for in vitro study. Cell proliferation and migration were assessed using MTT method and an in vitro wounding model, respectively. Transforming growth factor β (TGFβ) protein expression was determined using ELISA assay. Ornithine decarboxylase (ODC) and c-Myc mRNA expression profiles were determined using RT-PCR. Results: MTX treatment caused severe mucosal damage, significantly increased small intestine MDA levels, and decreased SOD and serum IgA levels in BALB/c mice. Gl-PS (100 and 200 mg/kg) markedly reversed the MTX effects. In IEC-6 cells, Gl-PS (0.1, 1, and 10 μg/mL) significantly stimulated the cell proliferation. Furthermore, Gl-PS (10 μg/mL) significantly stimulated the cell migration. In addition, Gl-PS (10 and 20 μg/mL) significantly increased the expression of ODC and c-Myc mRNAs. However, Gl-PS (up to 20 μg/mL) had no effect on the expression of TGFβ protein. Conclusion: The results suggest that Gl-PS protects small intestine against MTX-induced injury via induction of epithelial cell proliferation and migration. © 2011 CPS and SIMM All rights reserved. Source


Tang L.,Changsha Medical University | Chen B.,Chinese University of Hong Kong | Ma B.,Walvax Biotechnology | Nie S.,Kunming Medical University
Genetics and Molecular Research | Year: 2014

In this study, we investigated the association between 5 interferon regulatory factor-5 (IRF5) single nucleotide polymorphisms (SNPs) and autoimmune diseases using the Medline citation index. Twenty-eight studies with 74 comparisons, including 16 rheumatoid arthritis (RA), 43 systemic lupus erythematous (SLE), 2 juvenile idiopathic arthritis (JIA), 6 multiple sclerosis (MS), and 5 systemic sclerosis (SSc) studies, were examined in the meta-analysis. The SNP rs2004640 was significantly associated with SLE, MS, and SSc, but not with JIA [odds ratio (OR) = 1.06, 95% confidence interval (CI) = 0.90-1.24, P = 0.48] or RA (OR = 1.03, 95%CI = 0.95-1.11, P = 0.44). A significant association was observed between rs2280714 and SLE, MS, and SSc, but not RA (OR = 1.01, 95%CI = 0.94-1.09, P = 0.80). Rs10954213 was associated with the pathogenesis of SLE, RA, MS, and SSc. rs2070197 and the exon 6 insertion were significantly associated with SLE. Haplotypes containing rs2004640T and rs2280714T were significantly associated with an increased risk of SLE, but not with RA. This meta-analysis certified that IRF5 polymorphisms confer susceptibility to SLE, MS, and SSc. To further confirm the correlations between polymorphisms of IRF5 and autoimmune disease susceptibility, studies involving a larger number of patients worldwide are necessary. © FUNPEC-RP. Source

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